FOREWORD

Praise our thanks to Allah SWT for all his grace and grace so that we can
finish the tutorial B Blok 10. Sholawat as greetings always pour out to our lord,
the great prophet Muhammad and his family, friends and followers until the end of
the age.

We recognize that this tutorial report is far from perfect therefore we expect
constructive criticism and suggestions, in order to refine the next tasks.In
completing this tutorial task, we have much help, guidance and advice. On this
occasion express the respect and gratitude to:
1. dr. R.A. Tanzila ,M.Kes as our supervisor.
2. All Members and related parties in the production of this report.

May Allah SWT give a reward for all the charity given to all those who have
supported us and hopefully this tutorial report useful for us and the development of
science. Hopefully we are always in the protection of Allah SWT. Amin.

Palembang,24 December 2019

Author

1
 CHAPTER I
INTRODUCTION

1.1 Background
The Cardio Cerebrovascular Block is the tenth block in the third semester of the
Curriculum Based on Medical Education Competency at the Faculty of Medicine,
University of Muhammadiyah Palembang. On this occasion a case study tutorial
was carried out in scenario A which presented the case.

1.2 Purpose and Objectives

The purpose and objectives of this tutorial practicum material , namely :
1. As a tutorial group task report that is part of KBK learning system at the
Faculty of Medicine,University of Muhammadiyah Palembang .
2. Can resolve the case given in the scenario with the method of analysis and
learning of group discussion.
3. Achieve the objectives of the tutorial learning method and understand the
concepts of this scenario.

2
 BAB II
DISCUSSION

2.1 Data Tutorial

Supervisor : dr. R.A. Tanzila,M.Kes
Moderator : Dhia Luthafiyyah Utami
Desk Secretary : Della Marsellah
Board Secretary : Mona Regita Utami
Tutorial Time : 1. Tuesday, 24 December 2019
Time :13.00 until 15.00 WIB
2. Thursday, 26 December 2019
Time :13.00 until 15.00 WIB

Tutorial rules :
1. Switch the phone off or in silence.
2. Raise your hand when going to argument
3. Permission when going out of the room
4. Relax and watch as the tutor gives directions
5. During the tutorial takes care of attitude and speech

2.2 Scenario Case

“Heartful Cry”

Mrs.X a 65 years old house wife,brought to the emergency department with

a chief complain of pain in the left chest since 6 hours ago,while sweeping the
garden. The pain felton the left side of the chest,feels like being overwritten by
heavy load and radiating to the left hand and lower jaw. The complain were
followed with a cold sweat and nausea.Before being brought to the hospital,Mrs.X

3
drank some pain killer which she bought from the small shop and take some rest ,
but the symptoms were not reduced.
Mrs.X has a history of high blood pressure since 10 years ago,but didn’t visit
the doctor regularly.Mrs.X has experienced this kind of symptom before,but its
was reduced when she was resting.History of diabetes were denied.Familial
history of heart disease were denied,but there was a history of familial diabetes.
Physical Examination:
BH 160cm , BW 80 kg
Vital Sign : BP 140/90 mmHg,Pulse 65x/m reguler;RR 26x/m,T 36,6◦C.
Visual Analog Scale (VAS):6
Head: Pale faces,pale conjungtive(-),icteric sclera(-)
Neck: JVP 5-2 cm H2O
Thoraks:
Pulmo
Inspection : static,dynamic,left and right symetris
Plpation : left and right stem fremitus simetric
Percution : sonor left and right
Auscultation : vesiculer (+/+) normal,Ronki(-/-),wheezing(-/-)
Cor
Inspektion : ictus cordis (-)
Palpation : ictus cordis were palpable at ICS V two finger from lateral li
nea midclavicularis sinistra
Percution : left heart border at ICS V two finger wide from lateral linea m
idclavicularis sinistra,right heart border at linea parasternalis-
dextra,upper heart border at ICS II
Auscultation : HR 65x/m,regular,heart sound I and II normal,murmur(-),gal
llop(-)
Abdoment : hepar and lien were not palpable
Ekstremity : edema(-)

4
 Additional Examination

Thorax RO: CTR >50%

Laboratory Examination:
Hb 12,5g/dl; Leukosit 11.000/mm3 ; trombosit 305.000/mm3 ; BSS 135
mg/dl,Total cholesterol 350 mg%,triglyceride 195 mg% HDL 30mg% LDL 224
mg% ; CK NAC 1250 U/L, CK MB 55 U/L, Troponin I 0,5 mg/ml

2.3 Clarification of Terms

No Clarification Meaning
1 Cold sweat Perspiration the clear liquid secret by
the sweet glands. (Dorland)
2 Regular Normal of comforming the
rule.(Dorland)
3 Ictus Cordis The pulse felt at the point of
maximum impuls which is the point
on the precordium farthest outwarts
and downwarts fro the sternum at
which the cardiac impuls can be felt.
(Dorland)
4 Sonor Lungs tissue percussion normal
sounds. (Dorland)
5 Nausea Stomach queasiness the urge to vomit.
(Dorland)

5
6 Vesiculer Normal breath sound on pulmonary.
(Dorland)
7 CTR Cardio Thoracic Ratio is the ratio
between the transverse diameter of the
heart to the transverse diameter of the
thorax. (Dorland)
8 Wheezing High frequence breathing sound that
is hear at the end respiration.
(Dorland)
9 Ronki Whistling or snoring sound heard on
auscultation of the chest when the air
channels are partly
obstructed.(Dorland)
10 JVP Venous blood pressure measured in
the jugular vein.(Dorland)
11 CK MB A form of an enzyme found primarily
in heart muscle cells. (Dorland)
12 CK NAC Enzyme which is found primarily in
skeletal muscle,cardiac muscle,and
brain tissue. (Dorland)
13 Visual Analog Scale (VAS) A way to calculate the pain scale use
by medicine practitioner.(Dorland)
14 Dynamic Pertaining to or manifestation force.
(Dorland)
15 Static Maintenance of constan level.
(Dorland)
16 Troponin A complex of muscle protein which
when combine with calcium influence
tropomiosin to initiate contraction.

6
 (Dorland)
17 Gallop Disorders rhythm of the heart.
(Dorland)
18 Cor The heart is mayor organ in the
cardiovascular system . the heart is
vomit by muscular apex cordis and
basis right and left . (Dorland)
19 Edema Anabnormal accumulation of fluid
intercellular space in the body.
(Dorland)
20 HDL As good cholesterol because because
it removes cholesterol from the blood
stream and deposites in the liver.
(Dorland)
21 LDL Low Dencity Lipoprotein is one of the
five major groups of lipoprotein
which transport all fat molecules
around the body in the extracelullar
water. (Dorland)

2.4 Identification of problems

1. Mrs.X a 65 years old house wife,brought to the emergency department with a
chief complain of pain in the left chest since 6 hours ago,while sweeping the
garden. The pain felton the left side of the chest,feels like being overwritten by
heavy load and radiating to the left hand and lower jaw.
2. The complain were followed with a cold sweat and nausea.Before being brought
to the hospital,Mrs.X drank some pain killer which she bought from the small
shop and take some rest , but the symptoms were not reduced.
3. Mrs.X has a history of high blood pressure since 10 years ago,but didn’t visit
the doctor regularly.Mrs.X has experienced this kind of symptom before,but its

7
 was reduced when she was resting.History of diabetes were denied.Familial
history of heart disease were denied,but there was a history of familial diabetes.

4. Physical Examination:
BH 160cm , BW 80 kg
Vital Sign : BP 140/90 mmHg,Pulse 65x/m reguler;RR 26x/m,T 36,6◦C.
Visual Analog Scale (VAS):6
Head: Pale faces,pale conjungtive(-),icteric sclera(-)
Neck: JVP 5-2 cm H2O
Thoraks:
Pulmo
Inspection : static,dynamic,left and right symetris
Palpation : left and right stem fremitus simetric
Percution : sonor left and right
Auscultation : vesiculer (+/+) normal,Ronki(-/-),wheezing(-/-)
Cor
Inspektion : ictus cordis (-)
Palpation : ictus cordis were palpable at ICS V two finger from lateral li
nea midclavicularis sinistra
Percution : left heart border at ICS V two finger wide from lateral linea m
idclavicularis sinistra,right heart border at linea parasternalis-
dextra,upper heart border at ICS II
Auscultation : HR 65x/m,regular,heart sound I and II normal,murmur(-),gal
llop(-)
Abdoment : hepar and lien were not palpable
Ekstremity : edema(-)
5. Additional Examination

8
 Thorax RO: CTR >50%
Laboratory Examination:
Hb 12,5g/dl; Leukosit 11.000/mm3 ; trombosit 305.000/mm3 ; BSS 135
mg/dl,Total colesterol 350 mg%,triglyceride 195 mg% HDL 30mg% LDL 224
mg% ; CK NAC 1250 U/L, CK MB 55 U/L, Troponin I 0,5 mg/ml
2.5 Priority Problem
First identification because it is the main complain,where if it is not overcome it
will cause complication interfere with activities and can cause death.
2.6 Problem Analysis
1. Mrs.X a 65 years old house wife,brought to the emergency department with a
chief complain of pain in the left chest since 6 hours ago,while sweeping the
garden. The pain felt on the left side of the chest,feels like being overwritten by
heavy load and radiating to the left hand and lower jaw.
a.What is the anatomy,physiology and histology in this case ?
Answer :
Heart Anatomy
The heart is located in the mediastinal cavity of the thorax (thorax) between
the two lungs. The membrane lining the heart is called the pericardium
which consists of 2 layers:
1. Pericardium parietalis, the outer layer that attaches to the sternum and
lung lining.
2. Visceral pericardium, the surface layer of the heart itself which is also
called the epicardium.

9
Between the two layers there is a liquid pericardium as a lubricant that
works to reduce friction due to heart movement when pumping. The heart
wall consists of 3 layers: Epicardium (Pericardium, Myocardium, and
Endocardium).
The heart consists of 4 chambers, namely two thin-walled chambers called
the atrium (porch), and 2 thick-walled chambers called ventricles
(chambers).
1. Atrium
a. Atrium dextra
functions as a low-oxygen reservoir of blood from the entire body. The
blood flows through the superior vena cava, inferior vena cava, and
coronary sinus originating from the heart itself. From the right atrium then
the blood is pumped to the right ventricle.
b. Atrium sinistra
receives oxygen-rich blood from the lungs through 4 pulmonary veins.
Then blood flowed into the left ventricle. Between the two atria separated
by a partition called the atrial septum.
2. Ventricles
a. Ventricular dextra
receives blood from the right atrium which is then pumped into the lungs
through the pulmonary artery.
b. Ventricular sinistra
receives blood from the left atrium and then pumps it to the entire body
through the aorta. The two ventricles are separated by a partition called the
ventricular septum.
2. Heart valve
1) Atrioventricular valve
It is a valve located between the atrium and ventricle ... the valve
between the right atrium and the right ventricle has three leaf valves
called the trisuspidalis valve. While the valve is located between the left

10
 atrium and the left ventricle has two leaf valves called bicuspidalis valve
or mitral valve. AV valves allow blood to flow from each atrium to the
ventricles at the time of ventricular diastole, and prevent backflow to the
atrium during ventricular systole.
2) Semilunar Valves
Semilunar valves consist of pulmonary valves and aortic valves.
Pulmonary valve, located between the pulmonary artery and the right
ventricle. Aortic valve, located between the left ventricle and aorta. The
two semilunar valves consist of 3 valve leaves. The presence of a
semilunar valve allows blood to flow from each ventricle to the
pulmonary artery or aorta during ventricular systole, and prevents back
flow to the ventricles during ventricular diastole.
Blood vessels in the heart muscle consist of:
1. Coronary Artery
Coronary arteries are the first branch of systemic circulation. Coronary
circulation consists of the right coronary artery and left coronary artery.
The coronary artery empties into the upper aortic valve leaf called
"sinus valsava".
2. Heart veins
The distribution of the coronary veins is actually parallel with the
distribution of the coronary arteries. The cardiac venous system consists
of 3 parts: the venous vein, the anterior cardiac vein, the coronary sinus.
Physiology Heart
The heart is divided by the middle wall, or septum, into the left and right
sides. Each side functions as an independent pump consisting of an atrium
and a ventricle. The atrium receives blood returning to the heart from blood
vessels. The right side of the heart receives blood from the tissues and sends
it to the lungs for oxygenation. The left side of the heart receives newly
oxygenated blood in the lungs and pumps it to tissues throughout the body.

11
Starting from the right atrium, blood flows into the heart's right ventricle.
From here, blood is pumped through the pulmonary arteries into the lungs,
where the blood is oxygenated. From the lungs, blood flows to the left side
of the heart through the pulmonary vein. Blood vessels that travel from the
right ventricle to the lungs and back to the left atrium are known as
pulmonary circulation.
Blood from the lungs enters the heart through the left atrium and continues
into the left ventricle. Blood is pumped out of the left ventricle into a large
vein known as the aorta. The aorta branches off into a series of arteries that
get smaller and eventually become a tangle of capillaries. At the top, red
turns blue when blood flows through the capillaries, indicating that oxygen
has left the blood and diffuses into the tissues.
After leaving the capillaries, blood flows into the side of the circulating vein,
traveling from a small vein into an increasingly larger vein. Veins from the
upper part of the body combine to form the superior vena cava. Veins from
the lower part of the body combine to form inferior vena cava. Both vena
cava empty their contents into the right atrium. Blood vessels that carry
blood from the left side of the heart to the tissue and back to the right side of
the heart are known as systemic circulation.
Histology Heart
Endokardium:
Consists of a layer of flat endothelial cells, which are located on a thin layer
of sub-endothelial loose connective tissue containing elastin and collagen
fibers, in addition to smooth muscle cells.
Miokardium:
The tunica is the thickest in the heart and consists of heart muscle cells
arranged in layers that surround the heart chambers in the form of
complicated choices. Myocardium is much thicker in the ventricles than in
the atrium.

12
Epikardium:
The outside of the heart is coated by a layer of fried epithelium
(mesothelium) which is supported by a thin layer of connective tissue. Loose
sub-epicardial connective tissue layer contains veins, nerves and many
adipocytes.
Structural design of blood vessels
All blood vessels larger than a certain diameter have the same structural
features and show a general description of their construction. Blood vessels
generally consist of layers or tunica, as shown in the picture.
1.Intimate tunica:
It has one layer of endothelial cells, which is supported by a thin layer of
sub-endothelial loose connective tissue that sometimes contains smooth
muscle cells. In the arteries, the intima is separated from the tunica media
by an internal lamina elastica, the outer component of the intima. This
lamina, which is composed of elastin, has a gap that allows the diffusion
of substances to provide nutrients to the cells inside the vessel wall.
2.Media tunica
middle layer, consisting mainly of concentric layers of smooth muscle
cells arranged in a twisted shape. In arteries, media tunica has thinner
lamina elastica externa, which separates from tunica adventitia.
3.Adventitia tunica:
Consists mainly of collagen and elastin fibers. The adventisia layer
gradually merges with the stromal connective tissue of the organ where
the blood vessels are located. (Sherwood,2014)

13
b.What is the meaning Mrs.X a 65 years old house wife,brought to the
emergency deparment with a chief complain of pain in the left chest since 6
hours ago ,while sweeping the garden?
Answer :
the meaning is that chest pain experienced by ms.s.X is caused by a sudden
reduction in blood flow to the heart, so that oxygen supply to myocardial
cells decreases. Reduction of blood flow to myocardial cells can be caused
by a blockage in the coronary arteries. At the time of activity, oxygen
demand will increase but the coronary arteries are inadequate so that it will
cause ischemic myocardial cells and cause pain in the left chest.
(Abrams,2005)

c.What are the possible causes of pain in the left chest ?

Answer :
1. Stomach acid disorder
2. Pneumonia
3. Fraktur Costae
4. Coronary heart disease
5. Pericarditis
6. Heart valve abnormality
7. Ischemic
8. Heart rhythm abnormality.(Sudoyo,2009)

d.What is correlation between age and gender in this case?

Answer :
chest pain experienced by mrs.x is likely due to acute coronary syndrome.
Acute coronary syndrome is actually higher in men aged> 50 years, but in
women will follow after women enter the menopause. because at the time
of menopause there will be a decrease in estrogen levels. HORMONE
Estherogen is a hormone that functions as an LDL antioxidant, so this

14
 estrogen plays a role in the balance of LDL and HDL in the blood. LDL
can penetrate blood vessel walls in an oxidized state, if the hormone
estrogen decreases then LDL will be oxidized and can penetrate blood
vessel walls, then can form atherosclerosis and ultimately can cause acute
coronary syndrome.(Anand,S,2010)

e.What is the meaning the pain felt on the left side of the chest,feels like being
overwritten by heavy load and radiating to the left hand and lower jaw?
Answer :
The meaning is pain that is transferred pain which is pain that originateds in
one area of the body but felt in another area.Visceral pain is often transferred
to the dermatome which is supplied by the same spinal cord segment as the
pain viscus.If transferred to the surface of the body , the viscerl nerve is
generally limited to the dermatome segment.
In myocardial infraction,the pain spreads to the left arm .lower jaw to
metabolic accumulation and oxygen deficiency which stimulates sensory
nerve endings in the myocardium. (Anand,S,2010)

f.How is the patophysiology of pain in the left chest ?

Answer :
Risk factor (hypertension and dyslipidemia)→ high blood pressure causes
direct trauma to the walls of blood vessels → entry of subtances in the blood
(LDL) into the endothelium of blood vessels → monocytes enter and will
meet with LDL → LDL is eaten by monocytes (makrofag) → macrophages
secrete free radicals → LDL is oxidized → macrophages turn into foam cells
→ out other substances such as calcium → the part that calcium enters
becomes hard → atherosclerosis → connective tissue formed → forming a
thicker plaque → atherosclerosis plaque that causes vasocontriction →
occlusion (blockage) especially in the coronary arteries → coronary blood
flow is not strong → impaired supply of oxygen and nutrients → myocardial

15
 ischemia → decreased cardiac perfusion → myocardial cells compensate by
anaerpbic respiration → lactid acid production → cell PH decreases → this
change in myocardial cell metabolism → chest pain.(Roffi,et all,2016)

g.What is the risk factor of pain in the left chest?

Answer : :
risk factors that can be changed and that cannot be changed. There are four
factors biological risk of irreversible myocardial infarction, i.e. age, sex,
race, and family history. Other risk factors can still be changed, so
potentially slowing down the atherogenic process (Sudoyo,2009)
Factors that are These can be changed are hyperlipidemia, hypertension,
smoking, diabetes, obesity, psychosocial factors, fruit consumption, diet
and alcohol, andphysical activity (Sudoyo,2009)

h.What are the possible disease of pain in the left chest ?

Answer :
The possible disease of pain in the left chest in this case is coronary heart
disease

2. The complain were followed with a cold sweat and nausea.Before being brought
to the hospital,Mrs.X drank some pain killer which she bought from the small
shop and take some rest , but the symptoms were not reduced.
a.What is the meaning the complain were followed with a cold sweat and
nausea ?
Answer :
The meaning is body compensation. When hypertension occurs, cardiac
output will decrease, when cardiac output decreases, the body will
compensate in the form of sympathetic and parasympathetic nerve
activation. Activation of the sympathetic nervous system will increase heart
contraction so that cardiac output will increase, in addition to increasing

16
 heart contraction, the role of the sympathetic nervous system will make the
body become cold sweats. activation of the sympathetic nervous system will
suppress the parasympathetic system so that the parasympathetic nerve will
be activated. activation of the parasympathetic nervous system will suppress
n.vagus and nausea occur. (Prince,2005)

b.How is the patophysiology of cold sweat and nausea in this case?

Answer :
Mechanism of nausea
coronary atherosclerosis  the longer it will cause plaque rupture 
thrombus formation  thrombus will break down the intima layer so that it
comes in direct contact with blood flow  obstruction in the coronary
arteries whose function is to carry oxygen-rich blood to the myocardium 
oxygen supply to the myocardium decreases  myocardial infarction 
myocardium converts aerobic metabolism to anaerobic  release of
histamine, kinin, proteolytic enzymes  impulses in the afferent nerve fibers
in the anterior nerves and posterriors of the heart  have the same effect on
the stimulation of the afferent nerve fibers in the vagus nerve in the
gastrointestinal tract  nausea.(Newby,2008)
Mechanism of cold sweat
myocardial infraction in the anterior part of the heart which is corroded by
the left anterior coronary artery descendens stimulates sympathetic nerves
 Pressure on parasympathetic nerve  disruption digestive system 
Hyper secretion on sebasea gland  Cold Sweat (Newby,2008)

c.What is the etiology a cold sweat and nausea in this case?

Answer :
Etiology of cold sweat
1. Hyperthyroidism
2. Shock

17
 3. Diabetes
4. Increased symphatetic nerve activity
Etiology of nausea
1. Intraperitoneal
Obstruction problems like obstruction pylorik,obstruction colonic.
2. Extraperitoneal
Kardiopulmonary disease like cardiomyopathy and myocardial infraction.
(Sudoyo,2009)

d.What is the meaning before being brought to the hospital,Mrs.X drank some
pain killer which she bought from the small shop and take some rest but the
symptoms were not reduced?
Answer :
It is possible that the drugs taken are NSAID, as we know that NSAID is for
pain relief due to inflammation. whereas pain is felt by mrs.X due to
myocardial infarction (Acute Coronary syndrome).
Pain does not go away at rest because the blockage in blood vessels is large
so the supply of oxygen to the heart is not fulfilled even though the work of
the heart is not heavy. (Roffi,et all,2016)

e.What is the possible drug that mrs.x consumed ?

Answer :
Golongan NSAID : Asam mefenamat , ibuprofen, Paracetamol.

3. Mrs.X has a history of high blood pressure since 10 years ago,but didn’t visit
the doctor regularly.Mrs.X has experienced this kind of symptom before,but its
was reduced when she was resting.History of diabetes were denied.Familial
history of heart disease were denied,but there was a history of familial diabetes.
a.What is meaning mrs.x has a history of high blood pressure since 1o years
ago.but didn’t visit the doctor regularly?

18
 Answer :

High blood pressure is a risk factor for acute coronary syndrome.

Hypertension is a condition where an increase in cardiac output results in an
increase in peripheral defenses or peripheral resistance. Increased blood
pressure will increase afterload so that the heart's work increases. Increased
heart work will require greater oxygen in myocardial cells. However, on the
other hand, hypertension that persists and has lasted a long time and is not
well managed, will eventually lead to endothelial dysfunction. If endothelial
dysfunction has occurred, it will cause the formation of plaque on the walls
of blood vessels, which will block blood flow in the coronary arteries. This
causes an imbalance between myocardial oxygen demand and myocardial
oxygen supply, which will cause ischemic myocardial and eventually acute
coronary syndromes.(Anand.S,2010)

b.What is the correlation history of high blood pressure with her chief
complain?
Answer :
The correlation is hypertension can cause a process of sclerosis in the arterial
wall. This process will facilitate the formation of blood clots and weaken
blood vessels. so that blood vessels are easily broken and thrombus formed
the process of hardening of the arteries in the heart resulting in reduced
supply of oxygen to the myocardium which can increase the chance of
myocardial infraction. (Sudoyo,2009)

c.What is the meaning Mrs.X has experienced this kind of symptom

before,but its was reduced when she was resting ?
Answer :
the meaning of the symptoms mrs. X is a result of stable angina pectoris,
stable angina pectoris is a clinical syndrome in the form of discomfort in the

19
 chest, due to oxygen supply carried by coronary blood flow is insufficient
for myocardial oxygen demand. This occurs when myocardial oxygen
demand increases (for example due to physical work, emotions,
thyrotoxicosis, hypertension), or when coronary blood flow is reduced (for
example in spasm or coronary thrombus) (Sudoyono,2009)

d.What is the meaning history of diabetes were denied.Familial history of

heart disease were denied,but there was a history of familial diabetes?
Answer :
The meaning is she has a family history of DM, but she doesn’t have DM
disease and she has no family history of heart disease because coronary
heard disease is not hereditary disease.

4. Physical Examination:
BH 160cm , BW 80 kg
Vital Sign : BP 140/90 mmHg,Pulse 65x/m reguler;RR 26x/m,T 36,6◦C.
Visual Analog Scale (VAS):6
Head: Pale faces,pale conjungtive(-),icteric sclera(-)
Neck: JVP 5-2 cm H2O
Thoraks:
Pulmo
Inspection : static,dynamic,left and right symetris
Palpation : left and right stem fremitus simetric
Percution : sonor left and right
Auscultation : vesiculer (+/+) normal,Ronki(-/-),wheezing(-/-)
Cor
Inspektion : ictus cordis (-)
Palpation : ictus cordis were palpable at ICS V two finger from lateral li
nea midclavicularis sinistra
Percution : left heart border at ICS V two finger wide from lateral linea m

20
 idclavicularis sinistra,right heart border at linea parasternalis-
dextra,upper heart border at ICS II
Auscultation : HR 65x/m,regular,heart sound I and II normal,murmur(-),gal
llop(-)
Abdoment : hepar and lien were not palpable
Ekstremity : edema(-)
a.What is interpretation of physical examination in this case?
Answer :

Category Normal Interpretation

IMT  <18, 5= Less Weight IMT = BW/BH (m2)
 18,5-22,9 = Normal = 80/2,56
Weight = 31,25 (Obesity II)
 ≥23,0 = Over Weight
 23-24,9 =Risk of
Obesity
 25-29,9 = Obesity I
 ≥30 = Obesity II
TD TD = 140/90 mmHg
Hipertension Stage I
RR 16-24x/minute 26x/minute (Takipneu)
Pulse 60-100 x/minute 65/minute (normal)
VAS  0- <4 = Carefree Pain VAS 6
 4- <7 = Moderate Pain moderate pain
 7- 10 = Severe Pain
Head Pale Face Abnormal

Palpation : Cardiomegali
Ictus cordis

21
 were
palpable at
ICS V two
finger from
lateral linea
midclavicula
ris sinistra
Percution : Cardiomegali
Left heart
border at
ICS V two
finger wide
from lateral
linea
midclavicula
ris sinistra,
right heart
border at
linea
parasternalis
dextra, upper
heart border
at ICS II
(Swartz,Mark,2007)

b.How is the abnormal mechanism of physical examination in this case?

Answer :
Mechanism of tachypnea
coronary atherosclerosis -> the longer it will cause plaque rupture ->
thrombus formation -> thrombus will break down the intima layer so that it

22
comes in direct contact with blood flow -> obstruction in the coronary
arteries whose function is to carry oxygen-rich blood to the myocardium - ->
oxygen supply to the myocardium decreases -> myocardial infarction ->
decreases the force of contraction and the developing power of the heart
chamber -> volume of the buds decreases -> cardiac output decreases ->
compensates the body to meet oxygen demand -> increases breathing
speed.(Prince,2012)
Mechanism of Pale Face
Risk factors (hypertension, dyslipidemia) → atherosclerosis → coronary
obstruction → decreased blood flow → decreased O2 supply to the tissue mi
myocardial ischemic → acute myocardial infarction mi myocardial tissue
necrosis (irreversible) → leukocyte infiltration → decreased O2 supply to
the tissue mi myocardial ischemia → acute myocardial infarction →
myocardial tissue necrosis (irreversible) → leukocyte infiltration pasokan
scarred O2 supply to the tissue mi myocardial ischemia → acute myocardial
infarction → myocardial tissue necrosis (irreversible) decreased heart →
decreased COP → decreased blood flow to the systemic → pale face.
(Prince,2012)
Mechanism of Hypertension
Risk factors (hypertension, dyslipidemia) →atherosclerosis → coronary
obstruction → decreased blood flow → decreased O2 supply to tissues mi
myocardial ischemia → acute myocardial infarction jantung cardiac hypoxia
→ using anaerobic metabolism → decreased blood flow → decreased supply
of O2 to the tissue mi myocardial ischemia → acute myocardial infarction
→ cardiac hypoxia → using anaerobic metabolism → accumulation of lactic
acid and decreasing the release of O2 tissue others such as: histamine, kinin,
and proteolytic enzymes simp stimulation of excess sympathetic nerves →
stimulates SA node →increased cardiac work → pressure in the heart
increases → hypertension.
(Price, 2012)

23
 Mechanism of cardiomegaly
Risk factors (hypertension) → uncontrolled high blood pressure (10 years)
→ heart compensates → cardiomegaly.(Prince,2012)

c.How to do JVP examination?

Answer :
1.Position the patient to sleep without a pillow
2.Position the patient lying with the head making an angle of 30-45◦
3.Ask the patient to turn to the left
4.Identify the patient’s externa jugular vein while is clearly visible on the la
teral side of the neck. look for the highest pulsation in the jugular vein
with the index finger and thumb then release the distal jugular vein so that
pulsation of venous blood flow appears.
5. Identify the position of the patient’s angular sternum.
6. Measure the distance (in cm) between the highest pulsation of the externa
jugular vein to the angular sternum using 2 crossbar
7. Determine the distance from the plane through the angular sternum.
8. Do the interpretation of the measurement results.
Normal JVP: jugular venous pulsation height is more than 2cm indicating an
increase in jugular venous pressure,for example due to right heart failure.
Normal JVP = 5-2cm H2O. (Sudoyo,2009)

d.What is the interpretation of VAS ?

Answer :
Visual Analog Scale (VAS) Visual analog scale (VAS) is the most widely
used way to assess pain. Anamnesis is performed on the patient to describe
pain as mild, moderate or severe and can interfere with activity or not.

24
 Explanation :
0 : No pain
1-3 :Mild pain: the client can objectively communicate well.
4-6 :Moderate pain: The client objectively hissing, grinning, can indicate the
location of pain, can describe it, can follow orders properly.
7-9 : Severe pain: objectively the client sometimes cannot follow orders but
still responds to actions, can indicate the location of pain, cannot describe it,
cannot be overcome by changing the position of the long breath and
distraction.
In this case : moderate pain.(Faucy,2008)
5. Additional Examination

Thorax RO: CTR >50%

Laboratory Examination:

25
Hb 12,5g/dl; Leukosit 11.000/mm3 ; trombosit 305.000/mm3 ; BSS 135
mg/dl,Total colesterol 350 mg%,triglyceride 195 mg% HDL 30mg% LDL 224
mg% ; CK NAC 1250 U/L, CK MB 55 U/L, Troponin I 0,5 mg/ml
a.What is the interpretation of EKG ?
Answer :
Rhythm : sinus rhythm
Rate : HR 65x/m, regular
Hypertrophy : LVH
Morphology : Q pathological III AVF, ST-Depresi V1-V2 V3-V4, T-
Inverted III AVF.
Interpretation : Iskemik anteroseptal et inferior. Old Myocaldial Infraction
inferior. (Thaler.MS,2014)

b.What is the interpretation of Thorax RO in this case?

Answer :
The CTI (CardioThorax Index) results in cases showing> 50% with a
straight heart waist and signs of congestive pulmonary. If a CTI> 50% is
obtained, it is categorized as cardiomegaly.(Gray,Huon.2009)

c.What is the interpretation of laboratory examination?

Answer :
No Examination Result Normal Interpretation
Value
1 Hb 12,5 g/dl
2 Leukocytes 11.000/mm3 5.000- Leukocytosis
10.000/mm3
3 Platelets 305.000/mm3 140.000- Normal
450.000/mm3
4 BSS 135 mg/dl 80-120 mg/dl Normal

26
 5 Total Cholesterol 350 mg% 150-250mg% Dyslipidemia
6 Triglyceride 195 mg% <150mg% Dyslipidemia
7 HDL 30 mg% >65mg% Dyslipidemia
8 LDL 224 mg% <150mg% Dyslipidemia
9 CK NAC 1250 U/L 30-180 U/L Abnormal
10 CK MB 55 U/L <25 U/L Abnormal
11 Troponin I 0,5 U/L <0,1 U/L Abnormal
(Swartz,Mark,2007)

d.What is the abnormal mechanism of laboratory examination?

Answer :
Mechanism of Dyslipidemia
disorders of fat metabolism  deficiency of the enzyme lipoprotein 
hypercholestromia  (cholesterol,triglyceride.LDL,VDL and blood plasma
chylomicrons) increased.
Mechanism of CK MB increased
This type of enzyme is found in many tissues, especially muscle,
myocardium and brain. There are 3 types of creatine kinase isoenzymes and
are labeled M (muscular) and B (brain). Increased serum enzyme levels are a
reliable indicator of damage to the heart.
Mechanism of CK NAC increased
Increased CK levels can occur due to muscle injury because CK is an
enzyme that is released when a muscle injury occurs. The sudden appearance
of CK in serum suggests the origin of myocardium, especially in clinical
situations where patients experience chest pain and electrocardiogram
changes (Sacher, 2004).
Mechanism of Troponin I increased

27
 imbalance between oxygen demand and supply  myocardial infarction 
anaerobic  lactic acid accumulation  if it continues  tissue damage 
troponin will be released into the plasma (Sacher,2004)

6. How to diagnosis the disease in the case ?

Answer :
1. Anamnesis
1. Name : Mrs. X
2. Age : 65 years old
3. Profession : House wife
4. Complaint : Pain in the left chest since 6 hours ago, while sweeping
the garden. The pain felton the left side of the chest,feels like being
overwritten by heavy load and radiating to the left hand and
lower jaw. The complain were followed with a cold sweat and
nausea.Before being brought to the hospital,Mrs.X drank some pain
killer which she bought from the small shop and take some rest , but
the symptoms were not reduced.
5. History : High blood pressure since 10 years ago,but didn’t visit the
doctor regularly.Mrs.X has experienced this kind of symptom
before,but its was reduced when she was resting. There was a
history of familial diabetes.
2. Physical Examination

BH 160cm , BW 80 kg

Vital Sign : BP 140/90 mmHg,Pulse 65x/m reguler;RR 26x/m,T

36,6◦C.

Visual Analog Scale (VAS):6

Head: Pale faces,pale conjungtive(-),icteric sclera(-)

Neck: JVP 5-2 cm H2O

Thoraks:

28
 Pulmo

Inspection : static,dynamic,left and right symetris

Palpation : left and right stem fremitus simetric
Percution : sonor left and right
Auscultation : vesiculer (+/+) normal,Ronki(-/-),wheezing(-/-)
Cor
Inspektion : ictus cordis (-)
Palpation : ictus cordis were palpable at ICS V two finger from
laterallineamidclavicularis sinistra
Percution : left heart border at ICS V two finger wide from lateral
linea midclavicularis sinistra,right heart border at linea
parasternalis dextra,upper heart border at ICS II
Auscultation : HR 65x/m,regular,heart sound I and II normal,murmur
(-),gallop(-)
Abdoment : hepar and lien were not palpable
Ekstremity : edema(-)
3. Addult Examination
Electrocardiography (ECG) examination, Photo Thorax examination,
and laboratory examination.

7. What are the differential diagnosis of the disease ?

Answer :
NSTEMI STEMI
Thrombus partial occlusion overall occlusion
EKG ST depression ,T inverted ST Elevation
Enzym increased increased

8. What are the additional examination of the disease ?

Answer :
1. Coronary Angiography

29
 Describes the narrowing or blockage of the coronary arteries,usually
performed to measure cardiac chamber pressure and assess the fuction of the
left ventricle (ejection fraction)
2. Nuclear Imaging Examination
a. Talium evaluate myocardial blood flow and cardio status
b.Technetium : collected in the selik selis around the necrotic area .
(Sudoyono,2009)

9. What is the working diagnosis ?

Answer :
Acute Coronary Syndrome non elevation ST (NSTEMI) et causa
atherosclerosis (hypertension stage 1 and dyslipidemia)

a. What is the definition of disease in this case ?

Answer :
NSTEMI is a condition of myocardial infarction and this condition
can also be seen from an increase in cardiac enzymes. On ECG
examination. ST segment is accepted and T wave inversion (White
et al, 2012). In NSTEMI, thrombus formation has occurred due to
the formation of plaque that is mixed with platelet containers and
some cells such as red or white blood cells (Porth & Grossman,
2014). If needed, NSTEMI cannot be treated, eating will make the
thrombus enlarge and can cause hypoxia to necrosis of cells in the
heart.

b. What is the epidemiology of disease in this case ?

Answer :
The median age at the time of presentation for ACS in the United
States is 68 years. Males outnumber females by a 3:2 ratio. The
incidence of ACS in the United States is over 780,000, and of

30
 those, approximately 70% will have NSTEMI ( Basit, H,dkk,
2019)

c. What is the etiology and risk factor of disease in this case ?

Answer :
Etiology
NSTEMI is caused by a decrease in oxygen supply and an
increase in myocardial oxygen demand which is exacerbated by
coronary obstruction. NSTEMI occurs due to acute thrombosis
or coronary vasoconstrictive processes, resulting in myocardial
ischaemia and can cause nocrosis of myocardial tissue to a lesser
degree, usually limited to the subendocardium.
This situation can not cause ST segment elevation, but causes the
release of penandanecrosis. The most common cause is a
decrease in myocardial perfusion resulting from narrowing of the
coronary arteries caused by thrombus non-occlusive which has
developed in the atherosclerotic plaque disturbed.
Risk Factor
1.Risk factors that cannot be changed

a. Age

b. Gender

c. History of coronary heart disease

d. Heredity

e. Race

2. Risk factors that can be changed

1.Dyslipidemia
2. Hypertension
3. Smoking

31
 4. Obesity
5. a diet high in saturated fat
3. Causative Factors
a.Thrombus is not occlusive on existing plaques
The most common cause of ACS is a decrease in myocardial
perfusion due to narrowing of the coronary arteries as a result
of the thrombus present in atherosclerotic plaque which is
torn / broken and usually does not clog. Microembolism
(small emboli) from platelet aggregation and its components
from ruptured plaque, which results in small distal infarction,
is a cause of release of markers of myocardial damage in
many patients.
b.Dynamics obstruction
A rather rare cause is dynamic obstruction, which may be the
result of a continuous focal spasm in the segment of the
epicardial coronary arteries (angina prinzmetal). This spasm is
caused by hyper-contractility of vascular smooth muscle and /
or due to endothelial dysfunction.
c.Progressive mechanical obstruction
The third cause of SKA is severe constriction but not because
of spasm or thrombus. This occurs in a number of patients
with progressive atherosclerosis or with re-stenosis after
percutaneous coronary intervention (PCI).
d.Inflammation and / or infection
The fourth cause is inflammation, caused by infection-
related, which may cause arterial narrowing, plaque
destabilization, rupture and thrombogenesis. Macrophages
and T-lymphocytes in plaque walls increase the expression
of enzymes such as metalloproteinases, which can result in
plaque thinning and rupture, which in turn can lead to SKA.

32
 e.Precipitating factors or circumstances
The fifth cause is SKA which is a secondary result of the
precipitating conditions outside the coronary arteries. In
these patients there is a cause of narrowing of the coronary
arteries which results in limited myocardial perfusion, and
they usually suffer from chronic stable angina.
(Sudoyo,200)

d. What is the classification of disease in this case ?

Answer :
1. Unstable Angina Pectoris (APTS)
APTS is where the symptoms of ischemia match SKA,
without an increase in cardiac marker enzymes (CK-MB,
troponin) with or without ECG changes that show ischemia
(ST segment depression, T wave inversion and transient ST
segment elevation
Included in unstable angina are:
a) If the patient has angina that is new within 2 months, where
angina is quite severe and the frequency is more than 3 times
per day.
b) If the patient with angina is getting heavier, angina was
previously stable, but angina attacks occur more frequently
and have more pain but the precipitation factor is lighter.
c) Patients with bouts of resting angina.
2.Myocardial Infarction Without Elevation of ST Segment
(NSTEMI)
Myocardial infarction without ST (NSTEMI) elevation is the
same as unstable angina pectoris and management is the same.
However, NSTEMI is established by myocardial necrosis and
an increase in cardiac biomaker.

33
 3.Myocardial Infarction with ST Segment Elevation (STEMI)
Myocardial infarction is a picture of transmural myocardial
injury due to total occlusion of coronary arteries by
thrombus.(Sudoyono,2009)

e.What are the clinical manifestasions of diseases in this case ?

Answer :
a.Chest pain, lasts for at least 30 minutes while the attack is less
than that. Besides that in angina, the pain will disappear by resting
but it is different with NSTEMI.
b.Shortness of breath, caused by a sudden increase in end pressure
left ventricular diastolic, besides that feelings of anxiety can cause
hypervenntilation. In infarcts without symptoms of pain, shortness
of breath is a sign of significant left ventricular dysfunction
c.Gastrointestinal symptoms, increased vagal activity cause nausea
and vomiting, and are usually more frequent in inferior infarction,
and diaphragmatic stimulation in inferior infarction can also cause
obstruction.
d.Other symptoms include palpitations, dizziness, or syncope from
arrhythmia, anxiety.

f. How the patophysiology of diseases in this case ?

Answer :
NSTEMI can be caused by a decrease in oxygen supply and or an
increase in myocardial oxygen demand that is exacerbated by
coronary obstruction. NSTEMI can occur due to acute thrombosis
or coronary vasoconstriction processes. Acute thrombosis in the
coronary arteries begins with unstable plaque rupture. This unstable
plate usually has a large lipid core, low smooth muscle density, thin
fibrous cap and high tissue concentration. A ruptured fat core has a

34
 high concentration of cholesterol esters with a high proportion of
unsaturated fatty acids. At the location of plaque rupture can be
found cells and T lymphocytes which indicate an inflammatory
process. These cells will release proinflammatory cytokines such as
TNF α, and IL-6. Furthermore IL-6 stimulates the release of hsCRP
in the liver (Sudoyono Aru W, 2009).

10. How to treatment the disease in the case ?

Answer :
Pharmacology :
1. oxygen if saturation 02 peripheral<90%
2. Nitrate (sublingual): nitroglycerin 0.4 mg or isosorbide dinitrate (ISDN) 5
mg every 5 minutes→initial dose 1 mg / hour
3. Aspirin (chewed): dose 160-300 mg
4. Clopidogrel (swallowed): loading dose 300-600 mg and maintenance dose
1 x 75 mg.
5. Morphine (intravenously): initial dose 2-4 mg, can be increased 8 mg, and
repeated every 5-15 minutes.
Side effects: depression of the breath.
6. refer to a specialist . (Meine TJ,2005)
Synthesis :

Nitroglycerin

Nitroglycerin is a vasodilator that reduces myocardial oxygen demand by

decreasing ventricular preload via venodilation; it enhances myocardial
oxygen delivery by dilating large coronary arteries and improving
collateral flow to ischemic areas. Nitroglycerin should initially be given
sublingually or by buccal spray (0.3-0.6 mg) every 5 minutes for a total of
3 doses. If pain persists, the administration of intravenous (IV)
nitroglycerin should be initiated (initial rate of 5-10 μg/min with increases

35
of 10 μg/min every 3 to 5 minutes until symptoms are relieved or if
systolic blood pressure falls below 100 mm Hg). Topical or oral nitrates
can be used if the episode of pain has resolved, and they may replace IV
nitroglycerin if the patient has been pain-free for 12 to 24 hours. Absolute
contraindications to the use of nitroglycerin are hypotension or the use of
sildenafil within the previous 24 hours or of tadalafil within the previous
48 hours.(Meine TJ,2005)

Morphine and Other Analgesics

Morphine is recommended when ischemia-related symptoms are

unrelieved after 3 doses of nitroglycerin or when such symptoms recur
during treatment. In such cases, 1 to 5 mg of morphine sulfate can be
administered intravenously every 5 to 30 minutes as needed, with careful
monitoring of blood pressure and respiratory rate. Morphine acts as a
potent analgesic and anxiolytic; in addition, its hemodynamic effects may
be beneficial in treating UA/NSTEMI. The 2007 ACC/AHA guidelines
downgraded the recommendation for the use of morphine for
uncontrolled ischemic discomfort from class I to class IIa because data
from a large observational registry, although subject to uncontrolled
selection biases, suggested that the adjusted likelihood of death was
higher when morphine was used.

The ACC/AHA guidelines state that the use of nonsteroidal anti-

inflammatory drugs, both nonselective agents and cyclooxygenase-2
selective agents (except for aspirin), should be discontinued when a
patient presents with UA/NSTEMI because of the known cardiovascular
risks associated with these agents,and also because the EXTRACT-TIMI
25 (Enoxaparin and Thrombolysis Reperfusion for Acute Myocardial
Infarction Treatment—Thrombolysis In Myocardial Infarction 25) trial

36
 found that these agents were associated with an increased risk of adverse
cardiovascular events(Meine TJ,2005)

Aspirin.

Aspirin blocks the synthesis of thromboxane A2 by irreversibly inhibiting

cyclooxygenase 1, thereby diminishing platelet aggregation. Four
randomized trials have each demonstrated that, compared with placebo,
aspirin reduces the risk of death or MI by more than 50% for patients
presenting with UA/NSTEMI. The ACC/AHA guidelines recommend an
initial daily dose of 162 to 325 mg, followed by a daily dose of 75 to 162
mg for long-term secondary prevention. Absolute contraindications to
aspirin therapy include documented aspirin allergy (eg, asthma or
anaphylaxis), active bleeding, or a known platelet disorder. Clopidogrel is
a recommended alternative for patients who cannot tolerate aspirin.

Clopidogrel.

Clopidogrel is a thienopyridine derivative that blocks the P2Y12

adenosine diphosphate (ADP) receptor on platelets. This action decreases
platelet activation and aggregation, increases bleeding time, and reduces
blood viscosity. Therapy with clopidogrel and aspirin is recommended for
essentially all patients with UA/NSTEMI. (Gibson ,CM,2009)

11. What are the complications of the disease ?

Answer :
1. Arrythmia
2. Shock Cardyogenic
3. Pericarditis
4. Cardiac arrest
5. Heart Faillure
6. Acute Pulmonary Edema.(Harrison,2015)

37
12. What is the prognosis of the disease?
Answer :
Dubia.

13. What is the competence of general practicioner ?

Answer :
3B emergency department:
Doctor graduates are able to make a clinical diagnosis and provide
preliminary therapy in an emergency to save lives or prevent the severity and /
or disability in patients. Doctor graduates are able to determine the most
appropriate referral for subsequent patient management. Medical graduates
are also able to follow up after returning from a referral.(KKI,2006)

14. What is Islamic point of view in the case ?

Answer :
-And we make your sleep for rest ( Q.S Al- Baqarah : 9)
- Indeed, your Lord knows that you stand (pray) less than two-thirds of the
night, or one-half of the night or a third and (likewise) a group of people who
are with you. And Allah determines the measurements of night and day. Allah
knows that you cannot determine the time limits, so He gives you relief, so
read what is easy (for you) from the Qur'an. He knows that there will be those
among you who are sick and those who walk on the earth seeking some of
God's gifts; and other people who fight in the way of Allah, then read what is
easy (for you) from the Koran and establish prayer, pay alms and give loans to
Allah a good loan. And whatever good you do for yourself, surely you will get
it (reward) in the sight of Allah as the best and the greatest reward. And ask
forgiveness from Allah; surely Allah is Forgiving, Most Merciful ( q.s AL-
Muzamil : 20 )

38
2.7 Conclusiom
Mrs. X a65 years old house wife has pain in the left chest ,fells like being
overwritten by heavy load and radiating to the left hand and lower jaw because
ACS-NSTEMI et causa atherosclerosis (hypertension grade 1 and dyslipidemia)
2.8 Conceptual Framework

Risk Factor
(Hypertension stage 1
,dislipidemia)

Atherosclerosis

thrombus

Infark Miokard with predispotition factors

elevation segment ST (Activity)
(STEMI)

coronary artery occlusion

Myocardial Ischemic

myocardial infraction

Nausea pain left chest cold sweat

radiating left
hand and lowe
jaw

39
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